The purpose of our research project is to study the effects of endotoxic and hemorrhagic shock on mitochondrial energy metabolism. As contributing intracellular factors, tissue PO2, pH, pK, and PNa are measured by microelectrodes and lysosomal enzyme activities determined using biochemical assay techniques. As opposed to endotoxemia and hemorrhage, which induce inhibition of mitochondrial reactions, lysosomal enzyme release, and alterations in cellular cation concentrations and pH tissue hypoxia alone does not induce damage to mitochondria or lysosomes. On the contrary, hypoxia induces adaptation of the mitochondrial respiratory activity to a new, higher than normal maximal level by increasing the turnover of the respiratory enzyme system. This adaptation occurs in both acute and chronic hypoxia. Increased tissue oxygenation in normoxic or chronically hypoxic adult or newborn animals induces an opposite change in mitochondrial respiratory capacity. We have, thus, shown at various levels of the tissue oxygenation that mitochondrial metabolic capacity is very sensitively controlled by in vivo availability of oxygen.